Strain Name:

C3H/HeOuJ-MaoaTg(H2-K1-Ifnb1)8Seif/J

Stock Number:

014132

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Availability:

Cryopreserved - Ready for recovery

These H2-IFNB transgenic mice have the murine interferon beta 1 (Ifnb1) gene driven by a fragment of the histocompatibility 2, K1, K region (H2-K1) promoter. The transgene integrated into the X-linked monoamine oxidase A (Maoa) gene, replacing exons 2-3 and abolishing Maoa gene function. These mice may be useful for studying MAOA-related aggression and abnormal development of neural circuits under excess serotonin.

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names C3H/HeOuJ-MaoaTg(H2-K1*-Ifnb1)8Seif/J    (Changed: 04-MAR-11 )
Type Coisogenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
GenerationN12+F2pN1
Generation Definitions
 
Donating InvestigatorDr. Isabelle Seif,   Centre Natl de la Recherche Scientifique

Description
These H2-IFNB transgenic mice have the murine interferon beta 1 (Ifnb1) coding sequence driven by a fragment of the murine histocompatibility 2, K1, K region (H2-K1) promoter. The transgene integrated into the X-linked monoamine oxidase A (Maoa) gene, replacing exons 2-3 and abolishing Maoa gene function. Hemizygous males and homozygous females are viable, and fertile until at least 6 months. MAOA is a mitochondrial enzyme that oxidizes monoamine neurotransmitters and dietary monoamines. These mutants lack MAOA activity resulting in increased levels of serotonin, dopamine, and norepinephrine. Excess serotonin in these mice causes abnormal development of certain neural circuits, such as in the barrelfield. During the first two postnatal weeks, these mice successively exhibit increased trembling and head nodding, frantic running and falling over. Adult males exhibit increased aggression towards subordinate males, male intruders, and females during courtship. These changes are not attributable to expression of the Ifnb1 transgene. These mice may be useful for studying MAOA-related aggression and abnormal development of neural circuits under excess serotonin.

Development
The H2-IFNB transgene was designed with the murine interferon beta 1 (Ifnb1) gene driven by a histocompatibility 2, K1, K region (H2-K1) truncated promoter. The transgene was microinjected into fertilized C3H/HeOuJIco oocytes and mice from founder line 8 were bred to C3H/HeOuJIco mice. This transgene integrated into the X-linked monoamine oxidase A (Maoa) gene, replacing exons 2-3. These mice were backcrossed to C3H/HeOuJIco mice for at least 11 generations. Upon arrival at The Jackson Laboratory, transgenic mice were bred to C3H/HeOuJ inbred mice (Stock No. 000635) to establish the colony.

Control Information

  Control
   000635 C3H/HeOuJ
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Maoa
018589   129-MaoaK284stop/J
017340   129S-Maoatm1Shih/J
014134   B6;129S-MaoaK284stop Maobtm1Shih/J
View Strains carrying other alleles of Maoa     (3 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Monoamine Oxidase A; MAOA
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Brunner Syndrome   (MAOA)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

MaoaTg(H2-K1-Ifnb1)8Seif/Y

        involves: C3H/HeJ
  • homeostasis/metabolism phenotype
  • abnormal noradrenaline level
    • mutants have elevated levels in the brain   (MGI Ref ID J:26232)
  • abnormal serotonin level
    • mutants have elevated serotonin levels in their brains   (MGI Ref ID J:26232)
  • increased dopamine level
    • mutants show increased levels of dopamine in their brains   (MGI Ref ID J:26232)
  • behavior/neurological phenotype
  • abnormal behavior
    • in the open field test, adult mutants spend increased time in the center with hesitation about which direction to take (although if this is due to sensory or cognitive deficits or reduced fear is not known); for 12-week old mice, male mutants spent significantly greater time in the center than did controls   (MGI Ref ID J:26232)
    • between days 11 and 16, animals run frantically and fall over   (MGI Ref ID J:26232)
    • abnormal depression-related behavior
      • in the Porsolt's swim test, adult mutants make persistent attempts to escape, whereas controls spend more time floating; 9-week old male mutants spend significantly reduced time immobile in the water compared to control C3H animals   (MGI Ref ID J:26232)
    • abnormal eating behavior
      • i.p. injection of MAOB inhibitors into adult mutants disrupts feeding   (MGI Ref ID J:26232)
    • abnormal grooming behavior
      • i.p. injection of MAOB inhibitors into adult mutants disrupts self-grooming   (MGI Ref ID J:26232)
    • abnormal motor coordination/ balance
      • between days 5 and 10, when placed on a new surface, animals move backward instead of pivoting   (MGI Ref ID J:26232)
      • impaired balance
        • in a beam-walking test, adult mutants grasp the edge of the beam with their hindlimbs whereas C3H adults are sure footed   (MGI Ref ID J:26232)
      • impaired righting response
        • between days 5 and 10, animals display prolonged righting compared to C3H controls   (MGI Ref ID J:26232)
    • abnormal sleep pattern
      • between days 11 and 16, sleep is accompanied by violent shaking and jumps dispersing littermates   (MGI Ref ID J:26232)
    • abnormal social/conspecific interaction
      • i.p. injection of MAOB inhibitors into adult mutants disrupts social interaction   (MGI Ref ID J:26232)
      • abnormal sexual interaction
        • when males are placed with a nonreceptive female for 30 minutes, courtship is disrupted by episodes of grasping reflected by increased female squeaking compared with control C3H male courtship behavior   (MGI Ref ID J:26232)
      • abnormal social investigation
        • in resident-intruder paradigms, mutant males attacked intruders faster than C3H controls which displayed intense social investigation and home cage checking initially   (MGI Ref ID J:26232)
      • increased aggression towards males
        • in 6-12 week old animals, males housed in groups from time of weaning display offensive aggressive behavior, signified by bite wounds on genitals and rump: wounds are most apparent at 3 months of age   (MGI Ref ID J:26232)
    • head bobbing
      • neonates display intense head nodding behavior   (MGI Ref ID J:26232)
    • hunched posture
      • between days 11 and 16, mice have a hunched posture   (MGI Ref ID J:26232)
    • hyperresponsive
      • between days 5 and 10, animals display prolonged, stronger reactions to pinching   (MGI Ref ID J:26232)
    • increased aggression toward humans
      • between days 11 and 16, animals have a greater tendency to bite the experimenter   (MGI Ref ID J:26232)
    • increased fear-related response
      • between days 11 and 16, animals promptly dig to hide under shavings in response to moderate sound and movement   (MGI Ref ID J:26232)
  • nervous system phenotype
  • abnormal cerebral cortex morphology
    • somatosensory cortex of male mutant pups and adults display complete absence of cylindrical aggregates of granule cells (barrels) in layer IV   (MGI Ref ID J:26232)
  • increased dopamine level
    • mutants show increased levels of dopamine in their brains   (MGI Ref ID J:26232)

MaoaTg(H2-K1-Ifnb1)8Seif/Y

        involves: C3H/HeJ
  • homeostasis/metabolism phenotype
  • abnormal circulating hormone level
    • plasma corticosterone increase in cold, restraint, water deprivation and chronic variable stress is attenuated in knockouts compared to control C3H animals; psychosocial stress produces hypothalamic-pituitary-adrenal system activation to similar extent in control and mutant animals   (MGI Ref ID J:106365)
  • abnormal noradrenaline level
    • females have elevated levels in the brain   (MGI Ref ID J:26232)
  • abnormal serotonin level
    • females have elevated serotonin levels in their brains   (MGI Ref ID J:26232)
    • levels are 4- and 1.5-fold higher in the brainstem and cervical spinal cord at E20 compared to control C3H animals; at P5, levels are 8- and 3.5-fold higher in brainstem and spinal cord compared to controls; at E18.5. ther is a 4.8- and 6.5-fold increase in levels compared to C3H control   (MGI Ref ID J:78281)
  • increased dopamine level
    • females show increased levels of dopamine in their brains   (MGI Ref ID J:26232)
  • behavior/neurological phenotype
  • abnormal behavior
    • in the open field test, female adults spend increased time in the center with hesitation about which direction to take (although if this is due to sensory or cognitive deficits or reduced fear is not known); for 12-week old mice, both male and female mutants spent significantly greater time in the center than did controls   (MGI Ref ID J:26232)
    • between days 11 and 16, animals run frantically and fall over   (MGI Ref ID J:26232)
    • abnormal depression-related behavior
      • in the Porsolt's swim test, female adults make persistent attempts to escape, whereas controls spend more time floating; 9-week old female mutants spend significantly reduced time immobile in the water compared to control C3H animals   (MGI Ref ID J:26232)
    • abnormal eating behavior
      • i.p. injection of MAOB inhibitors into female adult mutants disrupts feeding   (MGI Ref ID J:26232)
    • abnormal grooming behavior
      • i.p. injection of MAOB inhibitors into female adult mutants disrupts self-grooming   (MGI Ref ID J:26232)
    • abnormal motor coordination/ balance
      • between days 5 and 10, when placed on a new surface, females move backward instead of pivoting   (MGI Ref ID J:26232)
      • impaired balance
        • between days 11 and 16, animals run frantically and fall over   (MGI Ref ID J:26232)
        • in a beam-walking test, female adults grasp the edge of the beam with their hindlimbs whereas C3H adults are sure footed   (MGI Ref ID J:26232)
      • impaired righting response
        • between days 5 and 10, animals display prolonged righting compared to C3H controls   (MGI Ref ID J:26232)
    • abnormal sleep pattern
      • between days 11 and 16, sleep in females is accompanied by violent shaking and jumps dispersing littermates   (MGI Ref ID J:26232)
    • abnormal social/conspecific interaction
      • i.p. injection of MAOB inhibitors into female adult mutants disrupts social interaction   (MGI Ref ID J:26232)
    • head bobbing
      • neonates display intense head nodding behavior   (MGI Ref ID J:26232)
    • hunched posture
      • between days 11 and 16, females have a hunched posture   (MGI Ref ID J:26232)
    • hyperresponsive
      • between days 5 and 10, females display prolonged, stronger reactions to pinching   (MGI Ref ID J:26232)
    • increased aggression toward humans
      • between days 11 and 16, females have a greater tendency to bite the experimenter   (MGI Ref ID J:26232)
    • increased fear-related response
      • between days 11 and 16, females promptly dig to hide under shavings in response to moderate sound and movement   (MGI Ref ID J:26232)
  • nervous system phenotype
  • abnormal cerebral cortex morphology
    • somatosensory cortex of female mutant pups and adults display complete absence of cylindrical aggregates of granule cells (barrels) in layer IV   (MGI Ref ID J:26232)
  • abnormal motor neuron morphology
    • in transgenic neonates, the dendritic morphology of the phrenic neurons is a multipolar tree rather than a bipolar dendritic tree in C3H controls; the number of distal dendrites is significantly greater in the transgenic neonates   (MGI Ref ID J:78281)
    • phrenic motor neurons in transgenics possess dendritic spines and swollen varicosities with a greater frequency than in C3H   (MGI Ref ID J:78281)
  • abnormal nervous system electrophysiology
    • in brainstem-spinal cord preparations from transgenic mice, isolated respiratory centers produce phrenic nerve bursts that are more variable in cycle duration and amplitude (quantified as coefficients of variability, CVd) than in C3H controls; treatment of dams with a 5-HT synthesis inhibitor from E18 to birth decreases the CVd variability in neonates   (MGI Ref ID J:78281)
    • treatment of pregnant control dams with a 5-HT receptor agonist from P18 to birth significantly increased the mean CVd of neonates compared to untreated controls, while treatment of pregnant mutant dams with a 5-HT receptor antagonist resulted in lowering of the CVd in P0-2 transgenic neonates compared to control transgenic neonates   (MGI Ref ID J:78281)
    • application of exogenous 5-HT to the medulla does not affect the phrenic burst frequency in P0-3 transgenic neonates, while in conrol C3H neonates, there is a dose-dependent increase in burst frequency   (MGI Ref ID J:78281)
  • increased dopamine level
    • females show increased levels of dopamine in their brains   (MGI Ref ID J:26232)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Developmental Biology Research
Internal/Organ Defects
      brain

Neurobiology Research
Behavioral and Learning Defects
Channel and Transporter Defects
Neurotransmitter Receptor and Synaptic Vesicle Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol MaoaTg(H2-K1-Ifnb1)8Seif
Allele Name transgene insertion 8, Isabelle Seif
Allele Type Transgenic (Inserted expressed sequence, Null/Knockout)
Common Name(s) MAO-A knockout; MAOA-KO; MaoaTg(H2-IFNB)8Seif; Tg8;
Mutation Made ByDr. Isabelle Seif,   Centre Natl de la Recherche Scientifique
Strain of OriginC3H/HeOuJ
Gene Symbol and Name Maoa, monoamine oxidase A
Chromosome X
Gene Common Name(s) 1110061B18Rik; AA407771; MAO-A; MGC:27811; Mao; RIKEN cDNA 1110061B18 gene; expressed sequence AA407771;
Molecular Note Random integration of a transgene for IFN beta expressed under the control of a truncated H2-K1 promoter resulted in deletion of a 17 kb region encompassing exons 2 and 3 of the Maoa gene. Enzyme activity was absent in brain and spleen samples from mutant animals. [MGI Ref ID J:26232]

Genotyping

Genotyping Information

Genotyping Protocols

MaoaTg(H2-K1-Ifnb1)8Seif, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Cases O; Seif I; Grimsby J; Gaspar P; Chen K; Pournin S; Muller U; Aguet M; Babinet C; Shih JC; De Maeyer E. 1995. Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA [see comments] Science 268(5218):1763-6. [PubMed: 7792602]  [MGI Ref ID J:26232]

Additional References

MaoaTg(H2-K1-Ifnb1)8Seif related

Agatsuma S; Lee M; Zhu H; Chen K; Shih JC; Seif I; Hiroi N. 2006. Monoamine oxidase A knockout mice exhibit impaired nicotine preference but normal responses to novel stimuli. Hum Mol Genet 15(18):2721-31. [PubMed: 16893910]  [MGI Ref ID J:115057]

Alvarez C; Vitalis T; Fon EA; Hanoun N; Hamon M; Seif I; Edwards R; Gaspar P; Cases O. 2002. Effects of genetic depletion of monoamines on somatosensory cortical development. Neuroscience 115(3):753-64. [PubMed: 12435414]  [MGI Ref ID J:120044]

Bou-Flores C; Lajard AM; Monteau R; De Maeyer E; Seif I; Lanoir J; Hilaire G. 2000. Abnormal phrenic motoneuron activity and morphology in neonatal monoamine oxidase A-deficient transgenic mice: possible role of a serotonin excess. J Neurosci 20(12):4646-56. [PubMed: 10844034]  [MGI Ref ID J:78281]

Bras H; Gaytan SP; Portalier P; Zanella S; Pasaro R; Coulon P; Hilaire G. 2008. Prenatal activation of 5-HT2A receptor induces expression of 5-HT1B receptor in phrenic motoneurons and alters the organization of their premotor network in newborn mice. Eur J Neurosci 28(6):1097-107. [PubMed: 18783379]  [MGI Ref ID J:142534]

Brown CE; Seif I; De Maeyer E; Dyck RH. 2003. Altered zincergic innervation of the developing primary somatosensory cortex in monoamine oxidase-A knockout mice. Brain Res Dev Brain Res 142(1):19-29. [PubMed: 12694941]  [MGI Ref ID J:83142]

Burnet H; Bevengut M; Chakri F; Bou-Flores C; Coulon P; Gaytan S; Pasaro R; Hilaire G. 2001. Altered respiratory activity and respiratory regulations in adult monoamine oxidase A-deficient mice. J Neurosci 21(14):5212-21. [PubMed: 11438596]  [MGI Ref ID J:110818]

Cases O; Lebrand C; Giros B; Vitalis T; De Maeyer E; Caron MG; Price DJ; Gaspar P; Seif I. 1998. Plasma membrane transporters of serotonin, dopamine, and norepinephrine mediate serotonin accumulation in atypical locations in the developing brain of monoamine oxidase A knock-outs. J Neurosci 18(17):6914-27. [PubMed: 9712661]  [MGI Ref ID J:49228]

Cases O; Vitalis T; Seif I; De Maeyer E; Sotelo C; Gaspar P. 1996. Lack of barrels in the somatosensory cortex of monoamine oxidase A-deficient mice: role of a serotonin excess during the critical period. Neuron 16(2):297-307. [PubMed: 8789945]  [MGI Ref ID J:31620]

Cazalets JR; Gardette M; Hilaire G. 2000. Locomotor network maturation is transiently delayed in the MAOA-deficient mouse. J Neurophysiol 83(4):2468-70. [PubMed: 10758149]  [MGI Ref ID J:62388]

Evrard A; Malagie I; Laporte AM; Boni C; Hanoun N; Trillat AC; Seif I; De Maeyer E; Gardier A; Hamon M; Adrien J. 2002. Altered regulation of the 5-HT system in the brain of MAO-A knock-out mice. Eur J Neurosci 15(5):841-51. [PubMed: 11906526]  [MGI Ref ID J:107998]

Ferrere A; Vitalis T; Gingras H; Gaspar P; Cases O. 2006. Expression of Cux-1 and Cux-2 in the developing somatosensory cortex of normal and barrel-defective mice. Anat Rec A Discov Mol Cell Evol Biol 288(2):158-65. [PubMed: 16419078]  [MGI Ref ID J:174183]

Gitton Y; Cohen-Tannoudji M; Wassef M. 1999. Role of thalamic axons in the expression of H-2Z1, a mouse somatosensory cortex specific marker. Cereb Cortex 9(6):611-20. [PubMed: 10498279]  [MGI Ref ID J:211471]

Holschneider DP; Scremin OU; Huynh L; Chen K; Seif I; Shih JC. 2000. Regional cerebral cortical activation in monoamine oxidase A-deficient mice: differential effects of chronic versus acute elevations in serotonin and norepinephrine. Neuroscience 101(4):869-77. [PubMed: 11113335]  [MGI Ref ID J:119047]

Holschneider DP; Scremin OU; Roos KP; Chialvo DR; Chen K; Shih JC. 2002. Increased baroreceptor response in mice deficient in monoamine oxidase A and B. Am J Physiol Heart Circ Physiol 282(3):H964-72. [PubMed: 11834493]  [MGI Ref ID J:75592]

Houades V; Koulakoff A; Ezan P; Seif I; Giaume C. 2008. Gap junction-mediated astrocytic networks in the mouse barrel cortex. J Neurosci 28(20):5207-17. [PubMed: 18480277]  [MGI Ref ID J:136320]

Kim JJ; Shih JC; Chen K; Chen L; Bao S; Maren S; Anagnostaras SG; Fanselow MS; De Maeyer E; Seif I; Thompson RF. 1997. Selective enhancement of emotional, but not motor, learning in monoamine oxidase A-deficient mice. Proc Natl Acad Sci U S A 94(11):5929-33. [PubMed: 9159177]  [MGI Ref ID J:40922]

Lairez O; Calise D; Bianchi P; Ordener C; Spreux-Varoquaux O; Guilbeau-Frugier C; Escourrou G; Seif I; Roncalli J; Pizzinat N; Galinier M; Parini A; Mialet-Perez J. 2009. Genetic deletion of MAO-A promotes serotonin-dependent ventricular hypertrophy by pressure overload. J Mol Cell Cardiol 46(4):587-95. [PubMed: 19162038]  [MGI Ref ID J:149172]

Lajard AM; Bou C; Monteau R; Hilaire G. 1999. Serotonin levels are abnormally elevated in the fetus of the monoamine oxidase-A-deficient transgenic mouse. Neurosci Lett 261(1-2):41-4. [PubMed: 10081922]  [MGI Ref ID J:55987]

Mossner R; Simantov R; Marx A; Lesch KP; Seif I. 2006. Aberrant accumulation of serotonin in dopaminergic neurons. Neurosci Lett 401(1-2):49-54. [PubMed: 16638624]  [MGI Ref ID J:144910]

Owesson CA; Hopwood SE; Callado LF; Seif I; McLaughlin DP; Stamford JA. 2002. Altered presynaptic function in monoaminergic neurons of monoamine oxidase-A knockout mice. Eur J Neurosci 15(9):1516-22. [PubMed: 12028362]  [MGI Ref ID J:107989]

Pchejetski D; Kunduzova O; Dayon A; Calise D; Seguelas MH; Leducq N; Seif I; Parini A; Cuvillier O. 2007. Oxidative stress-dependent sphingosine kinase-1 inhibition mediates monoamine oxidase A-associated cardiac cell apoptosis. Circ Res 100(1):41-9. [PubMed: 17158340]  [MGI Ref ID J:130242]

Popova NK; Maslova LN; Morosova EA; Bulygina VV; Seif I. 2006. MAO A knockout attenuates adrenocortical response to various kinds of stress. Psychoneuroendocrinology 31(2):179-86. [PubMed: 16112493]  [MGI Ref ID J:106365]

Popova NK; Vishnivetskaya GB; Ivanova EA; Skrinskaya JA; Seif I. 2000. Altered behavior and alcohol tolerance in transgenic mice lacking MAO A: a comparison with effects of MAO A inhibitor clorgyline. Pharmacol Biochem Behav 67(4):719-27. [PubMed: 11166062]  [MGI Ref ID J:128582]

Rebsam A; Seif I; Gaspar P. 2005. Dissociating barrel development and lesion-induced plasticity in the mouse somatosensory cortex. J Neurosci 25(3):706-10. [PubMed: 15659608]  [MGI Ref ID J:97681]

Rebsam A; Seif I; Gaspar P. 2002. Refinement of thalamocortical arbors and emergence of barrel domains in the primary somatosensory cortex: a study of normal and monoamine oxidase a knock-out mice. J Neurosci 22(19):8541-52. [PubMed: 12351728]  [MGI Ref ID J:79237]

Salichon N; Gaspar P; Upton AL; Picaud S; Hanoun N; Hamon M; De Maeyer E; Murphy DL; Mossner R; Lesch KP; Hen R; Seif I. 2001. Excessive activation of serotonin (5-HT) 1B receptors disrupts the formation of sensory maps in monoamine oxidase a and 5-ht transporter knock-out mice. J Neurosci 21(3):884-96. [PubMed: 11157075]  [MGI Ref ID J:67191]

Shih JC; Chen K. 1999. MAO-A and -B gene knock-out mice exhibit distinctly different behavior. Neurobiology 7(2):235-46. [PubMed: 10591056]  [MGI Ref ID J:59830]

St-Louis R; Parmentier C; Grange-Messent V; Mhaouty-Kodja S; Hardin-Pouzet H. 2014. Reactive oxygen species are physiological mediators of the noradrenergic signaling pathway in the mouse supraoptic nucleus. Free Radic Biol Med 71:231-9. [PubMed: 24681257]  [MGI Ref ID J:212124]

Stankovski L; Alvarez C; Ouimet T; Vitalis T; El-Hachimi KH; Price D; Deneris E; Gaspar P; Cases O. 2007. Developmental cell death is enhanced in the cerebral cortex of mice lacking the brain vesicular monoamine transporter. J Neurosci 27(6):1315-24. [PubMed: 17287506]  [MGI Ref ID J:118338]

Teskey GC; Radford KS; Seif I; Dyck RH. 2004. MAO(A) knockout mice are more susceptible to seizures but show reduced epileptogenesis. Epilepsy Res 59(1):25-34. [PubMed: 15135164]  [MGI Ref ID J:101841]

Thompson AM. 2008. Serotonin immunoreactivity in auditory brainstem neurons of the postnatal monoamine oxidase-A knockout mouse. Brain Res 1228:58-67. [PubMed: 18634763]  [MGI Ref ID J:139805]

Thompson AM; Thompson GC. 2009. Experimental evidence that the serotonin transporter mediates serotonin accumulation in LSO neurons of the postnatal mouse. Brain Res 1253:60-8. [PubMed: 19070605]  [MGI Ref ID J:147800]

Thompson AM; Thompson GC. 2009. Serotonin-immunoreactive neurons in the postnatal MAO-A KO mouse lateral superior olive project to the inferior colliculus. Neurosci Lett 460(1):47-51. [PubMed: 19446603]  [MGI Ref ID J:150575]

Upton AL; Salichon N; Lebrand C; Ravary A; Blakely R; Seif I; Gaspar P. 1999. Excess of serotonin (5-HT) alters the segregation of ispilateral and contralateral retinal projections in monoamine oxidase A knock-out mice: possible role of 5-HT uptake in retinal ganglion cells during development. J Neurosci 19(16):7007-24. [PubMed: 10436056]  [MGI Ref ID J:56671]

Vacher CM; Calas A; Maltonti F; Hardin-Pouzet H. 2004. Postnatal regulation by monoamines of vasopressin expression in the neuroendocrine hypothalamus of MAO-A-deficient mice. Eur J Neurosci 19(4):1110-4. [PubMed: 15009159]  [MGI Ref ID J:96499]

Vishnivetskaya GB; Skrinskaya JA; Seif I; Popova NK. 2007. Effect of MAO A deficiency on different kinds of aggression and social investigation in mice. Aggress Behav 33(1):1-6. [PubMed: 17441000]  [MGI Ref ID J:127892]

Vitalis T; Cases O; Gillies K; Hanoun N; Hamon M; Seif I; Gaspar P; Kind P; Price DJ. 2002. Interactions between TrkB signaling and serotonin excess in the developing murine somatosensory cortex: a role in tangential and radial organization of thalamocortical axons. J Neurosci 22(12):4987-5000. [PubMed: 12077195]  [MGI Ref ID J:77515]

Yang Z; Seif I; Armstrong-James M. 2002. Adult experience-dependent plasticity of S1 barrel cortex in the normal and monoamine oxidase-A knockout (Tg8) mouse. Cereb Cortex 12(12):1269-79. [PubMed: 12427678]  [MGI Ref ID J:102320]

Yang Z; Seif I; Armstrong-James M. 2001. Differences in somatosensory processing in S1 barrel cortex between normal and monoamine oxidase A knockout (Tg8) adult mice. Cereb Cortex 11(1):26-36. [PubMed: 11113033]  [MGI Ref ID J:102078]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, homozygous females may be bred to hemizygous males. Males are aggressive.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3300.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4290.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   000635 C3H/HeOuJ
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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